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Contents.ClassificationThe movement difficulties found in PD are called, which is defined as (slowness in initiating voluntary movements, with progressive reduction in speed and range of repetitive actions such as voluntary finger-tapping ) in combination with one of three other physical signs: muscular ( or ) rigidity, at rest,. A number of different disorders can have parkinsonism type movement issues.Parkinson's disease is the most common form of parkinsonism and is sometimes called 'idiopathic parkinsonism', meaning parkinsonism with no identifiable cause. Identifiable causes of parkinsonism include toxins, infections, side effects of drugs, metabolic derangement, and brain lesions such as strokes. Several neurodegenerative disorders also may present with parkinsonism and are sometimes referred to as 'atypical parkinsonism' or syndromes (illnesses with parkinsonism plus some other features distinguishing them from PD). They include, and (DLB).Scientists sometimes refer to Parkinson’s disease as a (due to an abnormal accumulation of protein in the brain) to distinguish it from other neurodegenerative diseases, such as where the brain accumulates. Considerable clinical and pathological overlap exists between and synucleinopathies. In contrast to Parkinson's disease, Alzheimer's disease presents most commonly with memory loss, and the cardinal signs of Parkinson's disease (slowness, tremor, stiffness, and postural instability) are not normal features of Alzheimer's.Dementia with Lewy bodies is another synucleinopathy and it has close pathological similarities with PD, especially with the subset of PD cases with known as.

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The relationship between PD and DLB is complex and incompletely understood. They may represent parts of a continuum with variable distinguishing clinical and pathological features or they may prove to be separate diseases. Signs and symptoms. Further information:Four motor symptoms are considered in PD: tremor, slowness of movement (bradykinesia), rigidity, and postural instability.The most common presenting sign is a coarse slow of the hand at rest which disappears during voluntary movement of the affected arm and in the deeper stages of sleep. It typically appears in only one hand, eventually affecting both hands as the disease progresses. Frequency of PD tremor is between 4 and 6 (cycles per second).

A feature of tremor is pill-rolling, the tendency of the index finger and thumb to touch and perform together a circular movement. The term derives from the similarity between the movement of people with PD and the early pharmaceutical technique of manually making pills.(slowness of movement) is found in every case of PD, and is due to disturbances in of movement initiation, and associated with difficulties along the whole course of the movement process, from planning to initiation to execution of a movement. Performance of sequential and simultaneous movement is impaired. Bradykinesia is the most handicapping symptom of Parkinson’s disease leading to difficulties with everyday tasks such as dressing, feeding, and bathing. It leads to particular difficulty in carrying out two independent motor activities at the same time and can be made worse by emotional stress or concurrent illnesses. Paradoxically patients with Parkinson's disease can often ride a bicycle or climb stairs more easily than walk on a level. While most physicians may readily notice bradykinesia, formal assessment requires a patient to do repetitive movements with their fingers and feet.is stiffness and resistance to limb movement caused by increased, an excessive and continuous contraction of muscles.

In parkinsonism the rigidity can be uniform (') or ratchety ('). The combination of tremor and increased tone is considered to be at the origin of cogwheel rigidity. Rigidity may be associated with joint pain; such pain being a frequent initial manifestation of the disease.

In early stages of Parkinson's disease, rigidity is often asymmetrical and it tends to affect the neck and shoulder muscles prior to the muscles of the face and extremities. With the progression of the disease, rigidity typically affects the whole body and reduces the ability to move.is typical in the later stages of the disease, leading to impaired balance and frequent falls, and secondarily to, loss of confidence, and reduced mobility. Instability is often absent in the initial stages, especially in younger people, especially prior to the development of bilateral symptoms. Up to 40% of people diagnosed with PD may experience falls and around 10% may have falls weekly, with the number of falls being related to the severity of PD.Other recognized motor signs and symptoms include gait and posture disturbances such as (rapid shuffling steps and a when walking with no flexed arm swing). Freezing of gait (brief arrests when the feet seem to get stuck to the floor, especially on turning or changing direction), a slurred monotonous quiet voice, mask-like facial expression, and handwriting that gets smaller and smaller are other common signs. NeuropsychiatricParkinson's disease can cause disturbances, which can range from mild to severe. This includes disorders of cognition, mood, behavior, and thought.Cognitive disturbances can occur in the early stages of the disease and sometimes prior to diagnosis, and increase in prevalence with duration of the disease.

The most common cognitive deficit in PD is, which can include problems with planning, abstract thinking, rule acquisition, initiating appropriate actions,. Other cognitive difficulties include, impaired and impaired perception and estimation of time. Nevertheless, improvement appears when recall is aided by cues.

Visuospatial difficulties are also part of the disease, seen for example when the individual is asked to perform tests of facial recognition and perception of the orientation of drawn lines.A person with PD has two to six times the risk of dementia compared to the general population. Up to 78% of people with PD have Parkinson's disease dementia.

The prevalence of dementia increases with age and, to a lesser degree, duration of the disease. Dementia is associated with a reduced in people with PD and their, increased mortality, and a higher probability of needing.Impulse control disorders including pathological gambling, compulsive sexual behavior, binge eating, compulsive shopping and reckless generosity can be caused by medication, particularly orally active dopamine agonists. The – with wanting of medication leading to overusage – is a rare complication of levodopa use.Behavior and mood alterations are more common in PD without cognitive impairment than in the general population, and are usually present in PD with dementia. The most frequent mood difficulties are,. Establishing the diagnosis of depression is complicated by the fact that the body language of depression may masquerade as PD including a sad expressionless anxious face, a hang dog appearance, slow movement, and monotonous speech.

Up to 30% of people with PD may experience symptoms of anxiety, ranging from a to,. They contribute to impaired quality of life and increased severity of motor symptoms such as on/off fluctuations or freezing episodes.in which complicated repetitive aimless occur for many hours is another disturbance caused by anti-Parkinson medication.or occur in approximately 50% of people with PD over the course of the illness, and may herald the emergence of dementia. These range from minor hallucinations – 'sense of passage' (something quickly passing beside the person) or 'sense of presence' (the perception of something/someone standing just to the side or behind the person) – to full blown vivid, and ideation. Auditory hallucinations are uncommon in PD, and are rarely described as voices. It is now believed that psychosis is an integral part of the disease. A psychosis with delusions and associated is a recognized complication of anti-Parkinson drug treatment and may also be caused by urinary tract infections (as frequently occurs in the fragile elderly), but drugs and infection are not the only factors, and underlying brain pathology or changes in neurotransmitters or their receptors (e.g., acetylcholine, serotonin) are also thought to play a role in psychosis in PD.

OtherIn addition to neuropsychiatric and motor symptoms, PD can impair other functions.are a feature of the disease and can be worsened by medications. Symptoms can manifest as daytime (including sudden sleep attacks resembling ), disturbances in sleep,. (RBD), in which patients act out dreams, sometimes injuring themselves or their bed partner, may begin many years before the development of motor or cognitive features of PD or.Alterations in the can lead to (low blood pressure upon standing), and excessive sweating, and altered sexual function. And can be severe enough to cause discomfort and even endanger health. Changes in perception may include an impaired sense of smell, disturbed vision, pain, and (tingling and numbness). All of these symptoms can occur years before diagnosis of the disease. Main article:Many risk factors have been proposed, sometimes in relation to theories concerning possible mechanisms of the disease; however, none have been conclusively proven.

The most frequently replicated relationships are an increased risk in those exposed to pesticides, and a reduced risk in smokers. There is a possible link between PD and infection that can prevent the absorption of some drugs including levodopa.

Environmental factorsExposure to and a history of head injury have each been linked with Parkinson disease (PD), but the risks are modest. Never having smoked cigarettes, and never drinking caffeinated beverages, are also associated with small increases in risk of developing PD.Low concentrations of in the blood is associated with an increased risk of PD. Parkin crystal structureResearch indicates that PD is the product of a complex interaction of genetic. Around 15% of individuals with PD have a who has the disease, and 5–10% of people with PD are known to have forms of the disease that occur because of a in one of several specific genes. Harboring one of these gene mutations may not lead to the disease; susceptibility factors put the individual at an increased risk, often in combination with other risk factors, which also affect age of onset, severity and progression.

At least 17 and have been implicated in the development of PD, including, and.About 5% of people with PD have mutations in the gene. These mutations are present in less than 1% of the unaffected population. The risk of developing PD is increased 20-30 fold if these mutations are present. PD associated with these mutations has the same clinical features, but an earlier age of onset and a more rapid cognitive and motor decline.SNCA gene mutations are important in PD because the protein which this gene encodes, is the main component of the that accumulate in the brains of people with PD. Activates ATM , a major repair signaling. In addition, alpha-synuclein activates the pathway. The aggregation of alpha-synuclein in appears to be a link between reduced and brain cell death in PDMutations in some genes, including SNCA, LRRK2 and GBA, have been found to be risk factors for 'sporadic' (non-familial) PD.

Mutations in the gene LRRK2 are the most common known cause of familial and sporadic PD, accounting for approximately 5% of individuals with a family history of the disease and 3% of sporadic cases. A mutation in GBA presents the greatest genetic risk of developing Parkinsons disease.Several Parkinson-related genes are involved in the function of, organelles that digest cellular waste products. It has been suggested that some cases of PD may be caused by that reduce the ability of cells to break down.An form has been associated with mutations in the gene. Schematic initial progression of Lewy body deposits in the first stages of Parkinson's disease, as proposed by Braak and colleagues. Localization of the area of significant brain in initial PD compared with a group of participants without the disease in a neuroimaging study, which concluded that damage may be the first identifiable stage of PDThere are five major pathways in the brain connecting other brain areas with the basal ganglia.

These are known as the, and circuits, with names indicating the main projection area of each circuit. All of them are affected in PD, and their disruption explains many of the symptoms of the disease, since these circuits are involved in a wide variety of functions, including movement, attention and learning. Scientifically, the motor circuit has been examined the most intensively.A particular conceptual model of the motor circuit and its alteration with PD has been of great influence since 1980, although some limitations have been pointed out which have led to modifications.

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In this model, the basal ganglia normally exert a constant inhibitory influence on a wide range of motor systems, preventing them from becoming active at inappropriate times. When a decision is made to perform a particular action, is reduced for the required motor system, thereby releasing it for activation. Dopamine acts to facilitate this release of inhibition, so high levels of dopamine function tend to promote motor activity, while low levels of dopamine function, such as occur in PD, demand greater exertions of effort for any given movement. Thus, the net effect of dopamine depletion is to produce, an overall reduction in motor output. Drugs that are used to treat PD, conversely, may produce excessive dopamine activity, allowing motor systems to be activated at inappropriate times and thereby producing. Brain cell deathThere is speculation of several mechanisms by which the brain cells could be lost.

One mechanism consists of an abnormal accumulation of the protein bound to in the damaged cells. This insoluble accumulates inside neurones forming inclusions called Lewy bodies.

According to the, a classification of the disease based on pathological findings proposed by, Lewy bodies first appear in the, and; individuals at this stage may be asymptomatic or may have early non-motor symptoms (such as loss of sense of smell, or some sleep or automatic dysfunction). As the disease progresses, Lewy bodies develop in the substantia nigra, areas of the and basal and, finally, the. These brain sites are the main places of neuronal degeneration in PD; however, Lewy bodies may not cause cell death and they may be protective (with the abnormal protein sequestered or walled off). Other forms of alpha-synuclein (e.g., ) that are not aggregated in Lewy bodies and may actually be the toxic forms of the protein. In people with dementia, a generalized presence of Lewy bodies is common in cortical areas. And, characteristic of, are not common unless the person is demented.Other cell-death mechanisms include and system dysfunction and reduced activity.

Iron accumulation in the substantia nigra is typically observed in conjunction with the protein inclusions. It may be related to, and neuronal death, but the mechanisms are not fully understood. DiagnosisA physician will initially assess for Parkinson's disease with a careful. People may be given levodopa, with any resulting improvement in motor impairment helping to confirm the PD diagnosis. The finding of Lewy bodies in the midbrain on is usually considered final proof that the person had PD. The clinical course of the illness over time may reveal it is not Parkinson's disease, requiring that the clinical presentation be periodically reviewed to confirm accuracy of the diagnosis.Other causes that can secondarily produce parkinsonism are and drugs. Such as and must be.

Anti-Parkinson's medications are typically less effective at controlling symptoms in Parkinson plus syndromes. Faster progression rates, early cognitive dysfunction or postural instability, minimal tremor or symmetry at onset may indicate a Parkinson plus disease rather than PD itself. Genetic forms with an autosomal or pattern of inheritance are sometimes referred to as familial Parkinson's disease or familial parkinsonism.Medical organizations have created to ease and standardize the diagnostic process, especially in the early stages of the disease. The most widely known criteria come from the UK Queen Square Brain Bank for Neurological Disorders and the U.S. The Queen Square Brain Bank criteria require slowness of movement (bradykinesia) plus either rigidity, resting tremor, or postural instability. Other possible causes of these symptoms need to be ruled out. Finally, three or more of the following supportive features are required during onset or evolution: unilateral onset, tremor at rest, progression in time, asymmetry of motor symptoms, response to levodopa for at least five years, clinical course of at least ten years and appearance of induced by the intake of excessive levodopa.When PD diagnoses are checked by autopsy, movement disorders experts are found on average to be 79.6% accurate at initial assessment and 83.9% accurate after they have refined their diagnosis at a follow-up examination.

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When clinical diagnoses performed mainly by nonexperts are checked by autopsy, average accuracy is 73.8%. Overall, 80.6% of PD diagnoses are accurate, and 82.7% of diagnoses using the Brain Bank criteria are accurate.A task force of the (MDS) has proposed diagnostic criteria for Parkinson’s disease as well as research criteria for the diagnosis of disease, but these will require validation against the more established criteria. Imaging(CT) scans of people with PD usually appear normal. Has become more accurate in diagnosis of the disease over time, specifically through iron-sensitive and sequences at a magnetic field strength of at least 3T, both of which can demonstrate absence of the characteristic 'swallow tail' imaging pattern in the. In a meta-analysis, absence of this pattern was highly and for the disease. Has shown potential in distinguishing between PD and Parkinson plus syndromes, though its diagnostic value is still under investigation.

CT and MRI are also used to rule out other diseases that can be secondary causes of parkinsonism, most commonly and, as well as less frequent entities such as basal ganglia and.The of in the basal ganglia can be directly measured with and scans, with the being a common proprietary version of this study. It has shown high agreement with clinical diagnoses of Parkinson's. Reduced dopamine-related activity in the basal ganglia can help exclude drug-induced Parkinsonism. This finding is not entirely specific, however, and can be seen with both PD and Parkinson-plus disorders. In the United States, DaTSCANs are only approved to distinguish Parkinson’s disease or Parkinsonian syndromes from. Differential diagnosisOther conditions that can have similar presentations to PD include. Drug induced parkinsonism.

Obsessional slowness. Psychogenic parkinsonism. Vascular parkinsonismPreventionExercise in middle age may reduce the risk of Parkinson's disease later in life.

Also appears protective with a greater decrease in risk occurring with a larger intake of caffeinated beverages such as coffee. People who smoke cigarettes or use are less likely than non-smokers to develop PD, and the more they have used tobacco, the less likely they are to develop PD. It is not known what underlies this effect. Tobacco use may actually protect against PD, or it may be that an unknown factor both increases the risk of PD and causes an aversion to tobacco or makes it easier to quit using tobacco., such as and, have been proposed to protect against the disease, but results of studies have been contradictory and no positive effect has been proven. The results regarding fat and have been contradictory, with various studies reporting protective effects, risk-increasing effects or no effects.

There have been preliminary indications that the use of drugs and may be protective. A 2010 found that (apart from ), have been associated with at least a 15 percent (higher in long-term and regular users) reduction of incidence of the development of Parkinson's disease.

Pharmacological treatment of Parkinson's diseaseThere is no cure for Parkinson's disease, but medications, surgery, and can provide relief and are much more effective than treatments available for other neurological disorders like Alzheimer’s disease,. The main families of drugs useful for treating motor symptoms are (always combined with a and sometimes also with a ),. The stage of the disease and the age at disease onset determine which group is most useful.of Parkinson's disease gives six stages, that can be used to identify early stages, later stages, and late stages. The initial stage in which some disability has already developed and requires pharmacological treatment is followed by later stages associated with the development of complications related to levodopa usage, and a third stage when symptoms unrelated to dopamine deficiency or levodopa treatment may predominate.Treatment in the first stage aims for an optimal between symptom control and treatment side-effects. The start of levodopa treatment may be postponed by initially using other medications such as MAO-B inhibitors and dopamine agonists instead, in the hope of delaying the onset of complications due to levodopa use. However, levodopa is still the most effective treatment for the motor symptoms of PD and should not be delayed in patients when their quality of life is impaired. Levodopa-related dyskinesias correlate more strongly with duration and severity of the disease than duration of levodopa treatment, so delaying this therapy may not provide much longer dyskinesia-free time than early use.In later stages the aim is to reduce PD symptoms while controlling fluctuations in the effect of the medication.

Sudden withdrawals from medication or its overuse have to be managed. When oral medications are not enough to control symptoms, surgery, subcutaneous waking day infusion and dopa pumps can be of use.

Late stage PD presents many challenges requiring a variety of treatments including those for psychiatric symptoms particularly, bladder dysfunction. In the final stages of the disease, is provided to improve quality of life. Medications LevodopaThe motor symptoms of PD are the result of reduced dopamine production in the brain's basal ganglia. Dopamine does not cross the, so it cannot be taken as a medicine to boost the brain's depleted levels of dopamine. However a of dopamine, levodopa, can pass through to the brain where it is readily converted to dopamine, and administration of levodopa temporarily diminishes the motor symptoms of PD. Levodopa has been the most widely used PD treatment for over 40 years.Only 5–10% of levodopa crosses the blood–brain barrier.

Much of the remainder is metabolized to dopamine elsewhere in the body, causing a variety of side effects including, vomiting. And are which do not cross the blood-brain barrier and inhibit the conversion of levodopa to dopamine outside the brain, reducing side effects and improving the availability of levodopa for passage into the brain.

One of these drugs is usually taken along with levodopa, often combined with levodopa in the same pill.Levodopa-use leads in the long term to the development of complications: involuntary movements called, and fluctuations in the effectiveness of the medication. When fluctuations occur, a person can cycle through phases with good response to medication and reduced PD symptoms ('on' state), and phases with poor response to medication and significant PD symptoms ('off' state). Using lower doses of levodopa may reduce the risk and severity of these levodopa-induced complications. A former strategy to reduce levodopa-related dyskinesia and fluctuations was to withdraw levodopa medication for some time. This is now discouraged since it can bring on dangerous side effects such as.

Most people with PD will eventually need levodopa and will later develop levodopa-induced fluctuations and dyskinesias.There are versions of levodopa. Older controlled-release levodopa preparations have poor and unreliable and and have not demonstrated improved control of PD motor symptoms or a reduction in levodopa-related complications when compared to immediate release preparations.

A newer extended-release levodopa preparation does seem to be more effective in reducing fluctuations but in many patients problems persist. Intestinal infusions of levodopa (Duodopa) can result in striking improvements in fluctuations compared to oral levodopa when the fluctuations are due to insufficient uptake caused. Other oral, longer acting formulations are under study and other modes of delivery (inhaled, transdermal) are being developed. COMT inhibitorsinhibits the activity, an enzyme which degrades dopamine. It has been used to complement levodopa; however, its usefulness is limited by possible complications such as liver damage. A similarly effective drug, has not been shown to cause significant alterations of liver function. Licensed preparations of entacapone contain entacapone alone or in combination with carbidopa and levodopa.

Dopamine agonistsSeveral that bind to dopamine receptors in the brain have similar effects to levodopa. These were initially used as a complementary therapy to levodopa for individuals experiencing levodopa complications (on-off fluctuations and dyskinesias); they are now mainly used on their own as first therapy for the motor symptoms of PD with the aim of delaying the initiation of levodopa therapy and so delaying the onset of levodopa's complications. Dopamine agonists include, and.Though dopamine agonists are less effective than levodopa at controlling PD motor symptoms, they are usually effective enough to manage these symptoms in the first years of treatment. Dyskinesias due to dopamine agonists are rare in younger people who have PD but, along with other complications, become more common with older age at onset.

Thus dopamine agonists are the preferred initial treatment for younger onset PD, and levodopa is preferred for older onset PD.Dopamine agonists produce significant, although usually mild, side effects including, hallucinations, insomnia, nausea, and constipation. Sometimes side effects appear even at a minimal clinically effective dose, leading the physician to search for a different drug. Agonists have been related to impulse control disorders (such as compulsive sexual activity, eating, gambling and shopping) even more strongly than levodopa. They tend to be more expensive than levodopa., a non-orally administered dopamine agonist, may be used to reduce off periods and dyskinesia in late PD. It is administered by intermittent injections or continuous.

Since secondary effects such as confusion and hallucinations are common, individuals receiving apomorphine treatment should be closely monitored. Two dopamine agonists that are administered through skin patches ( and ) and are useful for people in the initial stages and possibly to control off states in those in the advanced state. MAO-B inhibitors(, and ) increase the amount of dopamine in the basal ganglia by inhibiting the activity of (MAO-B), an enzyme which breaks down dopamine. Like dopamine agonists, their use may delay the commencement of levodopa therapy in early disease, but MAO-B inhibitors produce more adverse effects and are less effective than levodopa at controlling PD motor symptoms. There are few studies of their effectiveness in the advanced stage, although results suggest that they are useful to reduce fluctuations between on and off periods.

An initial study indicated that selegiline in combination with levodopa increased the risk of death, but this was later disproven. Main article:Other drugs such as and may be useful as treatment of motor symptoms. However, the evidence supporting them lacks quality, so they are not first choice treatments. In addition to motor symptoms, PD is accompanied by a diverse range of symptoms. A number of drugs have been used to treat some of these problems. Examples are the use of for psychosis, for dementia, and for. In 2016 was approved for the management of Parkinson's disease psychosis.Doxepin and rasagline may reduce physical fatigue in PD.

Placement of an electrode into the brain. The head is stabilised in a frame for.Treating motor symptoms with surgery was once a common practice, but since the discovery of levodopa, the number of operations has declined. Studies in the past few decades have led to great improvements in surgical techniques, so that surgery is again being used in people with advanced PD for whom drug therapy is no longer sufficient. Surgery for PD can be divided in two main groups: lesional and (DBS). Target areas for DBS or lesions include the, the or the. Deep brain stimulation is the most commonly used surgical treatment, developed in the 1980s by and others.

It involves the implantation of a medical device called a, which sends electrical impulses to specific parts of the brain. DBS is recommended for people who have PD with motor fluctuations and tremor inadequately controlled by medication, or to those who are intolerant to medication, as long as they do not have severe problems. Other, less common, surgical therapies involve intentional formation of lesions to suppress overactivity of specific areas.

For example, involves surgical destruction of the globus pallidus to control dyskinesia.Four areas of the brain have been treated with neural stimulators in PD. These are the, and the. DBS of the globus pallidus interna improves motor function while DBS of the thalamic DBS improves tremor but has little effect on bradykinesia or rigidity.

DBS of the subthalamic nucleus is usually avoided if a history of depression or neurocognitive impairment is present. DBS of the subthalamic nucleus is associated with reduction in medication. Pedunculopontine nucleus DBS remains experimental at present.

Generally DBS is associated with 30–60% improvement in motor score evaluations.Rehabilitation. Further information:Exercise programs are recommended in people with Parkinson's disease. There is some evidence that speech or mobility problems can improve with rehabilitation, although studies are scarce and of low quality. Regular with or without can be beneficial to maintain and improve mobility, flexibility, strength, gait speed, and quality of life. When an exercise program is performed under the supervision of a physiotherapist, there are more improvements in motor symptoms, mental and emotional functions, daily living activities, and quality of life compared to a self-supervised exercise program at home. In terms of improving flexibility and range of motion for people experiencing, generalized relaxation techniques such as gentle rocking have been found to decrease excessive muscle tension.

Other effective techniques to promote relaxation include slow rotational movements of the extremities and trunk, rhythmic initiation, and techniques. As for gait and addressing the challenges associated with the disease such as (slowness of movement), shuffling and decreased arm swing; physiotherapists have a variety of strategies to improve functional mobility and safety. Areas of interest with respect to gait during rehabilitation programs focus on, but are not limited to improving gait speed, the base of support, stride length, trunk and arm swing movement. Strategies include utilizing assistive equipment (pole walking and treadmill walking), verbal cueing (manual, visual and auditory), exercises (marching and PNF patterns) and altering environments (surfaces, inputs, open vs. Strengthening exercises have shown improvements in strength and motor function for people with primary muscular weakness and weakness related to inactivity with mild to moderate Parkinson's disease. However, reports show a significant interaction between strength and the time the medications was taken.

Therefore, it is recommended that people with PD should perform exercises 45 minutes to one hour after medications when they are at their best. Also, due to the forward flexed posture, and respiratory dysfunctions in advanced Parkinson's disease, deep diaphragmatic breathing exercises are beneficial in improving chest wall mobility and vital capacity. Exercise may improve constipation. It is unclear if exercise reduces physical fatigue in PD.One of the most widely practiced disorders associated with Parkinson's disease is the (LSVT). Speech therapy and specifically LSVT may improve speech. (OT) aims to promote health and quality of life by helping people with the disease to participate in as many of their as possible.

There have been few studies on the effectiveness of OT and their quality is poor, although there is some indication that it may improve motor skills and quality of life for the duration of the therapy. Palliative careis specialized medical care for people with serious illnesses, including Parkinson's. The goal of this speciality is to improve quality of life for both the person with Parkinson's and the family by providing relief from the symptoms, pain, and stress of illnesses. As Parkinson's is not a curable disease, all treatments are focused on slowing decline and improving quality of life, and are therefore palliative in nature.Palliative care should be involved earlier, rather than later in the disease course.

Palliative care specialists can help with physical symptoms, emotional factors such as loss of function and jobs, depression, fear, and existential concerns.Along with offering emotional support to both the patient and family, palliative care serves an important role in addressing goals of care. People with Parkinson's may have many difficult decisions to make as the disease progresses such as wishes for, and; wishes for or against; and when to use care. Palliative care team members can help answer questions and guide people with Parkinson's on these complex and emotional topics to help them make the best decision based on their own values.Muscles and nerves that control the digestive process may be affected by PD, resulting in and (food remaining in the stomach for a longer period than normal). A balanced diet, based on periodical nutritional assessments, is recommended and should be designed to avoid weight loss or gain and minimize consequences of gastrointestinal dysfunction. As the disease advances, swallowing difficulties may appear. In such cases it may be helpful to use for liquid intake and an upright posture when eating, both measures reducing the risk of choking.

To deliver food directly into the stomach is possible in severe cases.Levodopa and use the same transportation system in the intestine and the blood–brain barrier, thereby competing for access. When they are taken together, this results in a reduced effectiveness of the drug. Therefore, when levodopa is introduced, excessive is discouraged and well balanced is recommended.

In advanced stages, additional intake of low-protein products such as bread or pasta is recommended for similar reasons. To minimize interaction with proteins, levodopa should be taken 30 minutes before meals.

At the same time, regimens for PD restrict proteins during breakfast and lunch, allowing protein intake in the evening. 80PD invariably progresses with time.

A severity rating method known as the (UPDRS) is the most commonly used metric for clinical study. A modified version known as the MDS-UPDRS is also sometimes used. An older scaling method known as the (originally published in 1967), and a similar scale known as the Modified Hoehn and Yahr scale, have also been commonly used.

The Hoehn and Yahr scale defines five basic stages of progression.Motor symptoms, if not treated, advance aggressively in the early stages of the disease and more slowly later. Untreated, individuals are expected to lose independent after an average of eight years and be bedridden after ten years. However, it is uncommon to find untreated people nowadays. Medication has improved the prognosis of motor symptoms, while at the same time it is a new source of disability, because of the undesired effects of levodopa after years of use. In people taking levodopa, the progression time of symptoms to a stage of high dependency from caregivers may be over 15 years.

However, it is hard to predict what course the disease will take for a given individual. Age is the best predictor of disease progression. The rate of motor decline is greater in those with less impairment at the time of diagnosis, while cognitive impairment is more frequent in those who are over 70 years of age at symptom onset.Since current therapies improve motor symptoms, disability at present is mainly related to non-motor features of the disease. Nevertheless, the relationship between disease progression and disability is not linear. Disability is initially related to motor symptoms. As the disease advances, disability is more related to motor symptoms that do not respond adequately to medication, such as swallowing/speech difficulties, and gait/balance problems; and also to levodopa-induced complications, which appear in up to 50% of individuals after 5 years of levodopa usage.

Finally, after ten years most people with the disease have autonomic disturbances, sleep problems, mood alterations and cognitive decline. All of these symptoms, especially cognitive decline, greatly increase disability.The of people with PD is reduced. Are around twice those of unaffected people.

Cognitive decline and dementia, old age at onset, a more advanced disease state and presence of swallowing problems are all mortality. On the other hand, a disease pattern mainly characterized by tremor as opposed to rigidity predicts an improved survival. Death from is twice as common in individuals with PD as in the healthy population.In 2013 PD resulted in about 103,000 deaths globally, up from 44,000 deaths in 1990. The death rate increased from an average of 1.5 to 1.8 per 100,000 during that time.

63–109PD is the second most common after and affects approximately seven million people globally and one million people in the United States. The is about 0.3% in industrialized countries.

PD is more common in the elderly and rates rise from 1% in those over 60 years of age to 4% of the population over 80. The mean age of onset is around 60 years, although 5–10% of cases, classified as young onset PD, begin between the ages of 20 and 50. Males are more often affected than females at a ratio of around 3:2.

PD may be less prevalent in those of African and Asian ancestry, although this finding is disputed. Some studies have proposed that it is more common in men than women, but others failed to detect any differences between the two sexes. The of PD is between 8 and 18 per 100,000 person–years. The age adjusted rate of Parkinson's disease in Estonia is 28.0/100,000 person years. The Estonian rate has been stable between 2000 and 2019. Who made important contributions to the understanding of the disease and proposed its current name honoringSeveral early sources, including an, an medical treatise, the, and 's writings, describe symptoms resembling those of PD. After Galen there are no references unambiguously related to PD until the 17th century.

In the 17th and 18th centuries, several authors wrote about elements of the disease, including, and.In 1817 an English doctor, published his essay reporting six cases of paralysis agitans. An Essay on the Shaking Palsy described the characteristic resting tremor, abnormal posture and gait, paralysis and diminished muscle strength, and the way that the disease progresses over time. Early neurologists who made further additions to the knowledge of the disease include, and, and most notably, whose studies between 1868 and 1881 were a landmark in the understanding of the disease. Among other advances, he made the distinction between rigidity, weakness and bradykinesia.

He also championed the renaming of the disease in honor of James Parkinson.In 1912 described microscopic particles in affected brains, later named '. In 1919 reported that the substantia nigra was the main cerebral structure affected, but this finding was not widely accepted until it was confirmed by further studies published by in 1938. The underlying changes in the were identified in the 1950s, due largely to the work of on the neurotransmitter dopamine and on its role on PD. In 1997, alpha-synuclein was found to be the main component of Lewy bodies by, and others.Anticholinergics and surgery (lesioning of the or some of the basal ganglia structures) were the only treatments until the arrival of levodopa, which reduced their use dramatically.

Was first synthesized in 1911 by, but it received little attention until the mid 20th century. It entered clinical practice in 1967 and brought about a revolution in the management of PD.

By the late 1980s introduced by and colleagues at, France, emerged as a possible treatment. Society and culture Cost.

'Parkinson's awareness' logo with red tulip symbolThe costs of PD to society are high, but precise calculations are difficult due to methodological issues in research and differences between countries. The annual cost in the UK is estimated to be between £49 million and £3.3 billion, while the cost per patient per year in the U.S. Is probably around $10,000 and the total burden around $23 billion.

The largest share of direct cost comes from and nursing homes, while the share coming from medication is substantially lower. Indirect costs are high, due to reduced productivity and the burden on caregivers. In addition to economic costs, PD reduces of those with the disease and their caregivers. Advocacy11 April, the birthday of James Parkinson, has been designated as World Parkinson's Day.

A red tulip was chosen by international organizations as the symbol of the disease in 2005: it represents the James Parkinson Tulip, registered in 1981 by a Dutch horticulturalist. Advocacy organizations include the, which has provided more than $180 million in care, research and support services since 1982, which has distributed more than $115 million for research and nearly $50 million for education and advocacy programs since its founding in 1957 by William Black; the, founded in 1961; and the, founded in 1992. Notable cases. At the in, at the age of 64.

He had shown signs of parkinsonism from the age of 38 until his death.Actor has PD and has greatly increased the public awareness of the disease. After diagnosis, Fox embraced his Parkinson's in television roles, sometimes acting without medication, in order to further illustrate the effects of the condition. He has written two autobiographies in which his fight against the disease plays a major role, and appeared before the without medication to illustrate the effects of the disease.

Aims to develop a cure for Parkinson's disease. Fox received an in medicine from for his contributions to research in Parkinson's disease.Professional cyclist and Olympic medalist, who was diagnosed with young onset Parkinson's at age 40, started the in 2004 to support Parkinson's research, focusing on quality of life for people with the disease.Boxer showed signs of Parkinson's when he was 38, but was not diagnosed until he was 42, and has been called the 'world's most famous Parkinson's patient'. Whether he had PD or is unresolved. See also:There is little prospect of significant new PD treatments in the near future. Currently active research directions include the search for new of the disease and studies of the potential usefulness of, transplants and agents. Animal modelsPD is not known to occur naturally in any species other than humans, although animal models which show some features of the disease are used in research. The appearance of parkinsonism in a group of drug addicts in the early 1980s who consumed a contaminated batch of the synthetic led to the discovery of the chemical as an agent that causes parkinsonism in non-human primates as well as in humans.

Other predominant toxin-based models employ the insecticide, the herbicide paraquat and the fungicide. Models based on toxins are most commonly used in.

Rodent models that replicate various aspects of PD have been developed. The use of, creates a model of Parkinson's disease in rats by targeting and destroying dopaminergic neurons in the nigrostriatal pathway when injected into the substantia nigra.

Gene therapyGene therapy typically involves the use of a non-infectious (i.e., a such as the ) to shuttle genetic material into a part of the brain. The gene used leads to the production of an that helps to manage PD symptoms or protects the brain from further damage. In 2010 there were four clinical trials using gene therapy in PD. There have not been important adverse effects in these trials although the clinical usefulness of gene therapy is still unknown.

One of these reported positive results in 2011, but the company filed for bankruptcy in March 2012. Neuroprotective treatments.

Several chemical compounds, such as (chemical structure pictured) have been proposed as neuroprotectors in PD, but their effectiveness has not been proven.Investigations on are at the forefront of PD research. Several molecules have been proposed as potential treatments. However, none of them have been conclusively demonstrated to reduce degeneration.

Agents currently under investigation include, inhibitors (, ), (, )and. Preclinical research also targets. A that primes the human immune system to destroy, PD01A (developed by Austrian company, Affiris), has entered clinical trials in humans. In 2018 another vaccine, PRX002/RG7935, has passed stage I trials and has been supported for stage II trials. Cell-based therapies. Main article:Since early in the 1980s, or tissues have been used in, in which dissociated cells are injected into the substantia nigra in the hope that they will incorporate themselves into the brain in a way that replaces the dopamine-producing cells that have been lost. Although there was initial evidence of dopamine-producing cell transplants being beneficial, to date indicate that cell transplants produce no long-term benefit.

An additional significant problem was the excess release of dopamine by the transplanted tissue, leading to. Transplants are a recent research target, because stem cells are easy to manipulate and stem cells transplanted into the brains of rodents and monkeys have been found to survive and reduce behavioral abnormalities. Nevertheless, use of fetal stem cells is. It has been proposed that effective treatments may be developed in a less controversial way by use of taken from adults. Othertemporarily improves levodopa-induced dyskinesias. Its usefulness in PD is an open research topic.

Several have been proposed as possible treatments; however there is no evidence that or improve symptoms. There is no evidence to substantiate that and practice of, or, have any effect on the course of the disease or symptoms. And are natural sources of levodopa and are eaten by many people with PD; their intake is not free of risks as life-threatening adverse reactions have been described, such as the.The role of the and the in Parkinsons became a topic of study in the 2010s, starting with work in germ-free transgenic mice, in which from people with PD had worse outcomes. Some studies in humans have shown a correlation between patterns of in the gut flora in the people with PD, and these patterns, along with a measure of severity of constipation, could diagnose PD with a 90% specificity but only a 67% sensitivity. As of 2017 some scientists hypothesized that changes in the gut flora might be an early site of PD pathology, or might be part of the pathology.

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